Lowering expression of Epsin-3 inhibits migration and invasion of lung adenocarcinoma cells by inhibiting the epithelial–mesenchymal transition

• Published in: Scientific reports Vol. 14; no. 1; pp. 17069 - 11
• Main Authors: Li, Yunhe, Zhang, Pei, Tang, Guoxu, Zhong, Jiahui, Wang, Zhenghong, Zhu, Bing
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 24.07.2024; Nature Publishing Group; Nature Portfolio
• Subjects: 631/67; 631/80; A549 Cells; Adapter proteins; Adaptor Proteins, Vesicular Transport - genetics; Adaptor Proteins, Vesicular Transport - metabolism; Adenocarcinoma; Adenocarcinoma - genetics; Adenocarcinoma - metabolism; Adenocarcinoma - pathology; Adenocarcinoma of Lung - genetics; Adenocarcinoma of Lung - metabolism; Adenocarcinoma of Lung - pathology; beta Catenin - metabolism; Breast cancer; Cadherins - genetics; Cadherins - metabolism; Cancer; Cell Line, Tumor; Cell migration; Cell Movement - genetics; Clathrin; E-cadherin; EMT; Endocytosis; Epithelial-Mesenchymal Transition - genetics; EPN3; Female; Gene expression; Gene Expression Regulation, Neoplastic; Glioma; Homeobox; Humanities and Social Sciences; Humans; Invasion; Lung adenocarcinoma; Lung cancer; Lung carcinoma; Lung diseases; Lung Neoplasms - genetics; Lung Neoplasms - metabolism; Lung Neoplasms - pathology; Male; Metastases; Metastasis; Middle Aged; multidisciplinary; N-Cadherin; Neoplasm Invasiveness; Non-small cell lung carcinoma; Science; Science (multidisciplinary); Small cell lung carcinoma; Snail protein; Transcription factors; Tumor cells; Vimentin; Wnt protein; Wnt Signaling Pathway; Zinc finger proteins; β-Catenin; EPN3; Lung adenocarcinoma; EMT; Invasion
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/s41598-024-68193-1

The epithelial–mesenchymal transition (EMT) is a genetic reprogramming that tumor cells utilize for metastasis. Epsin-3 (EPN3) is an endocytic adapter protein involved in clathrin-mediated endocytosis and had been previously linked to EMT in breast cancer and glioma metastasis. In this study, identified the role of epsin-3 in lung adenocarcinoma and metastasis and epsin-3 levels identified using an expression profile analysis of patient data indicated the protein was abnormally overexpressed in lung adenocarcinoma patients and this was directly linked to disease severity. Gene knockdowns of EPN3 in human adenocarcinoma cell line A549 and the non-small cell lung carcinoma cell line H1299 decreased the levels of mesenchymal markers, including vimentin (VIM), N-cadherin (NCAD) and embryonic transcription factors like zinc finger E-box binding homeobox 1(ZEB1), snail, and the key molecules of Wnt pathway such as β-catenin and resulted in increased expression of the epithelial marker E-cadherin (ECAD). Our data links EPN3 to the EMT process in lung cancer and inhibition of its expression reduced the metastatic and invasive ability of lung adenocarcinoma cells by inhibiting the EMT process.